Inflammatory bowel disease (IBD) is associated with loss of immune tolerance to antigens originating from the diet and from the gut microflora. T cells play crucial roles in the pathogenesis of IBD. Chlorpyrifos (CPF) is one of the most ubiquitous organophosphate pesticides in the world. The aim of the study was to investigate the effects of dietary exposure to CPF on T-cell populations in C57BL/6 mice with dextran sulfate sodium (DSS)-induced colitis. Mice received distilled water containing 3% DSS for 6 days to induce acute colitis, which was then replaced with distilled water for 21 days, allowing progression to chronic inflammation. During the experimental period, mice were given either an AIN-93-based control diet or a CPF diet-containing 7, 17.5, or 35 ppm of CPF. Results showed that dietary exposure to CPF significantly increased circulating neutrophils in colitic mice. CPF-exposed groups had lower percentages of blood and spleen T cells without altering the proportions of CD4+ and CD8+ T-cell subsets. The percentage of blood regulatory T (Treg) cells, as well as splenic expressions of Treg-related genes, were suppressed in CPF-exposed mice. CPF upregulated the colonic gene expression of tumor necrosis factor-α. Meanwhile, plasma haptoglobin, colon weights, and luminal immunoglobulin G levels were higher in CPF-exposed groups. Histopathological analyses also observed that colon injury was more severe in all CPF-exposed mice. These results suggest that dietary exposure to CPF aggravated tissue injuries in mice with DSS-induced chronic colitis by suppressing T-cell populations and Treg polarization.

中文翻译：

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饮食中毒死rif可抑制硫酸葡聚糖硫酸钠诱导的结肠炎的C57BL / 6小鼠中调节性T细胞的极化。

炎症性肠病（IBD）与对饮食和肠道菌群产生的抗原的免疫耐受性下降有关。T细胞在IBD的发病机理中起着至关重要的作用。毒死rif（CPF）是世界上最普遍的有机磷农药之一。该研究的目的是研究饮食中CPF暴露对硫酸葡聚糖硫酸钠（DSS）诱导的结肠炎对C57BL / 6小鼠T细胞群体的影响。小鼠接受含有3％DSS的蒸馏水治疗6天，以诱发急性结肠炎，然后将其替换为蒸馏水21天，从而发展为慢性炎症。在实验期间，给小鼠喂食基于AIN-93的对照饮食或含有7、17.5或35 ppm CPF的CPF饮食。结果表明，饮食中CPF的暴露显着增加了结肠炎小鼠的循环中性粒细胞。CPF暴露组的血液和脾T细胞百分比较低，而不会改变CD4 +和CD8 + T细胞亚群的比例。在暴露于CPF中的小鼠中，血液调节性T（Treg）细胞的百分比以及Treg相关基因的脾脏表达受到抑制。CPF上调了肿瘤坏死因子-α的结肠基因表达。同时，CPF暴露组的血浆触珠蛋白，结肠重量和管腔免疫球蛋白G水平较高。组织病理学分析还观察到所有CPF暴露小鼠的结肠损伤更为严重。这些结果表明，饮食中CPF的暴露通过抑制T细胞数量和Treg极化，加剧了DSS诱发的慢性结肠炎小鼠的组织损伤。